Eur J Appl Physiol DOI 10.1007/s00421-008-0773-z ORIGINAL ARTICLE End-tidal pressure of CO2 and exercise performance in healthy subjects Maurizio Bussotti Æ Damiano Magrı̀ Æ Emanuele Previtali Æ Stefania Farina Æ Anna Torri Æ Marco Matturri Æ Piergiuseppe Agostoni Accepted: 12 May 2008 Ó Springer-Verlag 2008 Abstract High arterial CO2 pressure (PaCO2) measured in athletes during exercise suggests inadequate hyperventilation. End-tidal CO2 pressure (PETCO2) is used to estimate PaCO2. However, PETCO2 also depends on exer_ 2 ) and ventilation cise intensity (CO2 production, VCO efficiency (being PETCO2 function of respiratory rate). We evaluated PETCO2 as a marker, which combines efficiency of ventilation and performance. A total of 45 well-trained volunteers underwent cardiopulmonary tests and were grouped according to PETCO2 at respiratory compensation (RC): Group 1 (PETCO2 35.1–41.5 mmHg), Group 2 (41.6–45.7) and Group 3 (45.8–62.6). At anaerobic _ threshold, RC and peak exercise, ventilation (VE) was similar, but in Group 3, a greater tidal volume (Vt) and lower respiratory rate (RR) were observed. Peak exercise _ 2 were lowest in Group 1 and similar workload and VO between Group 2 and 3. Group 3 subjects also showed high _ 2 suggesting a greater glycolytic metabolism. In peak VCO M. Bussotti (&) D. Magrı̀ S. Farina M. Matturri P. Agostoni Centro Cardiologico Monzino, IRCCS, Istituto di Cardiologia, Università degli Studi di Milano, Via Parea 4, 20138 Milan, Italy e-mail: [email protected] D. Magrı̀ Dipartimento di Scienza Cardiovascolari, Respiratorie e Morfologiche, Università La Sapienza, Rome, Italy E. Previtali A. Torri Istituto di Medicina Interna II, Università degli Studi di Milano, Milan, Italy P. Agostoni Division of Respiratory and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, WA, USA conclusion, a high PETCO2 during exercise is useful in identifying a specific respiratory pattern characterized by high tidal volume and low respiratory rate. This respiratory pattern may belong to subjects with potential high performance. Keywords Exercise Athletes End tidal of CO2 Ventilation Introduction Many studies have gathered data suggesting ventilatory limitations of aerobic exercise in athletes. Excessive alveolar to arterial O2 pressure (DPA-aO2) difference, abnormal increases in arterial CO2 pressure (PaCO2) and haemoglobin desaturation have been demonstrated (Dempsey and Wagner 1999; Durand et al. 2000; Rodman et al. 2002). A high value of PaCO2 suggests an inadequate ventilation increase during exercise. This phenomenon may be due to mechanical respiratory constraint, on reaching the upper limit of expiratory flow rate and/or respiratory muscle force production (Johnson et al. 1992), or to a low chemoreceptor responsiveness (Harms and Stager 1995). However, a lower hyperventilation and the consequent higher PaCO2 can, per se, affect maximal exercise performance. Indeed, a reduced hyperventilation could determine lower respiratory muscles work allowing for a lower blood flow towards respiratory muscles and a gain of up to 10%, in leg blood flow (Harms et al. 1997, 1998, 2000). This mechanism delays the onset of leg fatigue and permits greater exercise performance. Furthermore, a higher PaCO2 is associated with greater tissue and blood acidosis, which through a rightward shift on the HbO2 saturation curve allows greater O2 delivery to muscles. 123 Eur J Appl Physiol End-tidal pressure of CO2 (PETCO2) is used for a noninvasive estimate of PaCO2 (Benallal and Busso 2000; Wasserman et al. 2005). During exercise, the difference between PaCO2 and PETCO2 is mainly related to respiratory rate (RR) because expiratory CO2 does not reach a plateau. Consequently, for a given alveolar CO2, higher the PETCO2 the lower is the RR. It is worthy to note that a high RR means low ventilation efficiency, since the higher the RR the greater is the percentage of dead space/tidal volume ventilation. Therefore, PETCO2 derives from muscle metabolism (amount of CO2 production), from the respiratory rate (RR) and CO2 chemoreceptor set point. Accordingly, in normal subjects, high PETCO2 may be due to high exercise performance and efficiency of ventilation. Consequently PETCO2 can be proposed as a marker, which combines performance and efficiency of ventilation. The aim of this paper is to evaluate, in healthy welltrained subjects, if during exercise a relationship between physical performance/efficiency of ventilation and PETCO2 exists. _ 2 ) increase and confirmed by specific behaviour of O2 (VCO _ VO _ 2 ) and CO2 (VE/ _ VCO _ 2 ) ventilatory equivalents and (VE/ end-tidal pressure of O2 (PETO2) and PETCO2 (Beaver et al. 1986). The end of respiratory compensation (RC) was _ VCO _ 2 increased and PETCO2 identified when VE/ _ decreased (Beaver et al. 1986; Wasserman 1978). VE/ _ VCO2 is reported both as the slope of the relationship, and measured from the beginning of loaded exercise to RC, and _ VCO _ 2 ratio. at each exercise workload, as the actual VE/ _ 2 /DWorkRate (WR) slope was measured The DVO throughout the entire exercise (Wasserman et al. 2005). We divided our study population into three groups according to PETCO2 values at RC: Group 1 (1st tertile: from 35.1 to 41.5 mmHg), Group 2 (2nd tertile: from 41.6 to 45.7 mmHg), Group 3 (3rd tertile: from 45.8 to 62.6 mmHg). The investigation was approved by the local ethics committee and subjects signed a written informed consent before participating in the study. Statistical analysis Methods A total of 45 healthy, physically well-trained volunteers participated in the study. We defined ‘‘well-trained’’ subjects as those who had been performing aerobic exercise on a regular basis for at least 1 year. Immediately before exercise testing, all subjects underwent standard lung function measurements (Vmax 29C, SensorMedics, USA). A maximal symptom-limited cardiopulmonary exercise test was performed on an electronically braked cycloergometer (Ergometrics-800, SensorMedics, USA), with the subject wearing a nose clip and breathing through a mass flow sensor (Vmax 29C, SensorMedics, USA) connected to a saliva trap. A personalized ramp exercise protocol was chosen, aiming at a test duration of &10 min. The exercise was preceded by 5 min of resting breath-bybreath gas exchange monitoring (rest) and by a 3 min unloaded warm-up. A 12-lead ECG, blood pressure and heart rate were also recorded. Tests were evaluated by two expert readers. The anaerobic threshold (AT) was identified by V-slope anal_ 2 ) and production of CO2 ysis of consumption of O2 (VO Data are reported as mean ± sd. Mean values of the cardiopulmonary exercise tests are results of 20 s averages. All data were evaluated with SPSS-PC + 13.0 statistical software (SPSS-PC + Inc, Chicago, Illinois). We compared all cardiopulmonary data of three groups at Rest, AT, RC and at peak exercise (Peak). The same data were also analysed at iso-workloads (50, 100, 150 and 200 W), where 200 W was the highest workload reached by all subjects. All comparisons were made by one-way ANOVA followed by a paired t-test as appropriated (Bonferroni post hoc analysis). A P value of \0.05 was considered to indicate statistical significance. Results All three groups were well matched with respect to age, gender and BMI (Table 1). The forced expiratory volume in the first second (FEV1) (107 ± 13, 105 ± 8 and 111 ± 9% of predicted in Group 1, 2 and 3, respectively, P = NS) and the forced vital capacity (FVC) (113 ± 14, 113 ± 9 and 112 ± 7% of predicted in Table 1 Demographics parameters of the study population Groups Gender (male/female) P = 0.330 Age (years) 22.6 ± 2.0 P = 0.180 69.7 ± 8.5 Height (cm) 1 12/2 12/3 38 ± 8 23.1 ± 3.3 70.2 ± 10.5 174.4 ± 5.5 3 16/0 33 ± 11 24.3 ± 2.3 76.7 ± 8.2 177.7 ± 6.8 123 P = 0.275 Weight (kg) 2 P = ANOVA test result 39 ± 10 BMI (kg/m2) P = 0.071 175.6 ± 7.9 P = 0.399 P \ 0.001 Group 2 vs. Group 1 P \ 0.001 Group 3 vs. Group 1, Group 1, 2 and 3 respectively, P = NS) between groups were similar. At Rest, a significant difference between groups was found only for PETCO2 (Table 2, Figure 1). Figure 1 _ 2 versus PETCO2 at Rest, AT, reports the behaviour of VO RC and Peak: Group 3 showed a significantly higher PETCO2 at all stages of exercise. Workload, heart rate (HR) and ventilatory parameters at all stages of exercise under examination are reported in Table 2. AT was reached by all subjects under similar workload and metabolic conditions (Table 2). At this step, we _ with, however, different ventilatory observed similar VE patterns between groups: indeed Vt progressively increased and RR reduced from Group 1 to Group 3. RC was reached at a progressively higher workload from Group 1 to 3 (Table 2). At this stage, the difference in _ 2 became significant. HR, workload, Vt and VO _ 2 and VCO _ 2 differences At Peak, HR, workload, Vt, VO were maintained (Table 2), but no differences in peak HR, _ 2 were observed between Group 2 and 3. workload and VO Peak exercise respiratory exchange ratio (RER) is reported in Fig. 2; RER is higher in Group 3 with respect to the other two groups (1.12 ± 0.11, 1.10 ± 0.07 and 1.23 ± 0.15 in Group 1,2 and 3, respectively; P = 0.005). _ 2 , expressed as percentage of VO _ 2 MAX predicted Peak VO by height, age and sex was: 113 ± 20, 132 ± 16 and 127 ± 16% in Group 1, 2 and 3, respectively (P = 0.013), showing a lower exercise performance in Group 1 and similar performances in Group 2 and 3. P \ 0.05 Group 3 vs. Group 2; P = ANOVA test result; * P \ 0.05 Group 3 vs. Group 1; 181 ± 15* 3 115.0 ± 22.5 349 ± 50 $ P \ 0.05 Group 2 vs. Group1, 48.0 ± 7.1* 39 ± 11 3.12 ± 0.51* & P \ 0.001 Group 3 vs. Group 2, § 45.2 ± 5.3& 59.4 ± 10.0 P = 0.000 39.0 ± 3.3 P = 0.001 36.5 ± 2.5 P = 0.014 46.7 ± 8.3 52.0 ± 6.4 48.8 ± 6.5$ P = 0.006 41.8 ± 6.6 P = 0.310 2.59 ± 0.54 2.59 ± 0.45 44 ± 8 112.6 ± 26.6 P = 0.025 104.4 ± 21.5 P = 0.455 41 ± 9 353 ± 70$ P = 0.006 298 ± 53 165 ± 14 178 ± 9$ 2 168 ± 15* 3 Peak 1 43.4 ± 7.1* 82.0 ± 19.2 308 ± 55* 28 ± 7 3.00 ± 0.63 32.7 ± 18.5 50.2 ± 4.5& P = 0.000 43.9 ± 1.4§ P = 0.229 38.8 ± 1.9 P = 0.036 35.4 ± 6.4 27.8 ± 4.8 42.7 ± 7.0 P = 0.022 37.3 ± 5.9 P = 0.190 2.58 ± 0.50 2.47 ± 0.48 31 ± 5 82.8 ± 18.8 P = 0.470 33 ± 7 75.2 ± 16.8 P = 0.022 254 ± 39 154 ± 15 165 ± 11 1 2 RC 138 ± 19 3 P = 0.027 299 ± 64 2.38 ± 0.71 49.1 ± 11.8 199 ± 53 22 ± 5* 31.3 ± 6.7 19.4 ± 10.1 49.6 ± 3.8& P = 0.000 P = 0.403 40.1 ± 2.3 43.9 ± 1.9$ 18.2 ± 3.3 P = 0.304 21.6 ± 5.4 P = 0.045 28.2 ± 7.8 32.2 ± 7.2 1.96 ± 0.40 P = 0.042 1.89 ± 0.53 25 ± 5 50.3 ± 13.1 P = 0.932 28 ± 8 P = 0.163 171 ± 50 129 ± 14 141 ± 14 1 2 AT 67 ± 5 3 P = 0.154 48.5 ± 13.0 5.3 ± 1.4 0.88 ± 0.21 15 ± 2 13.1 ± 4.2 – 210 ± 57 4.7 ± 1.6 37.6 ± 3.1* P = 0.005 35.6 ± 2.4 P = 0.153 33.8 ± 3.4 4.7 ± 1.9 3.8 ± 0.5 P = 0.464 4.8 ± 0.7 5.1 ± 1.1 P = 0.431 0.88 ± 0.49 0.70 ± 0.12 16 ± 3 – P = 0.104 16 ± 5 12.7 ± 3.8 10.6 ± 1.1 P = 0.140 – 68 ± 4 72 ± 6 1 2 Rest RR (breath/min) _ (l/min) VE Work (Watt) Groups HR (bpm) Table 2 Cardiopulmonary data at metabolic steps in the three study groups divided according to PETCO2 values Vt (l) P = 0.184 _ 2 /kg (ml/kg/min) VO _ 2 /kg (ml/kg/min) VCO Pet CO2 (mmHg) Eur J Appl Physiol _ 2 ) and end-tidal pressure of CO2 Fig. 1 O2 consumption (VO (PETCO2) behaviour at Rest, at anaerobic threshold (AT), at end of respiratory compensation (RC) and at Peak in the three study groups. _ 2 and PETCO2 between The standard deviation and ANOVA for VO groups are given in the table inset. Continuous line, long dashed line and short dashed line identify respectively Group 1, 2 and 3. _ 2 values of Group 1. _ 2 values of Group 3 vs. VO *P \ 0.05 VO $ _ 2 values of Group 2 vs. VO _ 2 values of Group 1 P \ 0.05 VO 123 123 26.6 ± 5.5 28.7 ± 5.4 P \ 0.001 Group 3 vs. & P \ 0.05 Group 3 vs. Group 2; 25 ± 5 22 ± 6 48.3 ± 5.4 49.3 ± 7.4 2 3 P = ANOVA test result; * P \ 0.05 Group 3 vs. Group 1; Group 2, $ P \ 0.05 Group 2 vs. Group 1 1.97 ± 0.30 2.31 ± 0.55 P \ 0.001 Group 3 vs. Group 1; 31.0 ± 3.7 31.0 ± 4.3 § P \ 0.001 Group 2 vs. Group 1, 26.5 ± 1.1 22.7 ± 2.2& P = 0.000 $ 29.1 ± 2.2 30.2 ± 5.9 30.9 ± 4.0 2.04 ± 0.33 30 ± 6 § 60.2 ± 9.7 1 200 P = 0.000 P = 0.000 20 ± 5* 36.0 ± 5.9 3 P = 0.002 1.90 ± 0.41 P = 0.060 23.4 ± 3.7 P = 0.996 20.4 ± 6.7 P = 0.224 23.5 ± 1.8& P = 0.000 27.5 ± 2.2 29.4 ± 2.9 22.1 ± 4.7 19.1 ± 3.6 25.0 ± 4.1 24.5 ± 3.6 1.69 ± 0.29 1.63 ± 0.27 35.9 ± 3.3§ 27 ± 8 23 ± 4 44.4 ± 7.4 2 150 P = 0.015 1 18 ± 4* 26.5 ± 3.1* 3 P = 0.004 1.60 ± 0.62 P = 0.079 16.8 ± 2.7 P = 0.457 13.7 ± 2.7 P = 0.179 25.7 ± 2.6& P = 0.000 30.7 ± 2.3 29.2 ± 2.0 13.5 ± 3.0 14.6 ± 2.7 17.9 ± 2.2 18.7 ± 2.6 1.47 ± 0.43 1.40 ± 0.28 20 ± 5 27.0 ± 3.6 2 23 ± 5 30.9 ± 5.9 1 100 20 ± 5 P = 0.296 P = 0.033 1.33 ± 0.35 16 ± 3* 20.4 ± 4.2 3 P = 0.525 10.6 ± 1.3 P = 0.128 9.4 ± 1.7 P = 0.534 28.6 ± 3.5 34.4 ± 3.7 32.2 ± 2.7 P = 0.331 9.0 ± 2.0 8.5 ± 1.5 P = 0.334 11.2 ± 1.5 11.3 ± 1.6 1.08 ± 0.38 1.09 ± 0.33 18.9 ± 3.8 2 P = 0.032 19 ± 4 21.5 ± 5.4 1 50 Vt (l) RR (breath/min) _ (l/min) VE The main finding of our study is that in a group of healthy physically well-trained subjects, those with the lowest values of PETCO2 during exercise have a low exercise _ 2 performance, as demonstrated by lower workload and VO reached. Interestingly these subjects showed a specific _ due to a high RR. ventilatory pattern, featuring high VE Group 2 and 3 subjects have the same exercise capacity, but subjects with the highest PETCO2 have also the highest _ 2 at peak exercise. VCO Groups Discussion Work (Watt) Data at iso-workloads are reported in Table 3. Differences in ventilatory pattern were observed at all stages. To evaluate the respiratory pattern throughout the exercise we also averaged all data obtained every 50 W (from 50 to 200 _ was where data from all subjects were obtained). Mean VE $ * 39.3 ± 16.3, 32.5 ± 11.7 and 33.0 ± 12.2 l/min, mean Vt was 1.56 ± 0.46, 1.54 ± 0.47 and 1.78 ± 0.61* l/min, mean RR was 25.1 ± 7.0, 21.7 ± 5.0$ and 19.0 ± 5.2 bpm in Group 1, 2 and 3 respectively. _ VCO _ 2 slope was 30.1 ± 2.8, 25.4 ± 2.3§ and The VE/ 22.0 ± 3.6 in Group 1, 2 and 3, respectively _ 2 /DWorkRate slope was 9.1 ± (P \ 0.0001). The DVO 0.9, 9.3 ± 1.8 and 9.5 ± 1.0 ml/W/min in Group 1, 2 and 3, respectively (P = 0.614) (* P \ 0.05 Group 3 vs. Group 1; $ P \ 0.05 Group 2 vs. Group 1; P \ 0.05 Group 3 vs. Group 2; P \ 0.001 Group 3 vs. Group 1; P \ 0.05 Group 3 vs. Group 2; § P \ 0.001 Group 2 vs. Group 1). Table 3 Iso-watt cardiopulmonary data in the three study groups divided according to PETCO2 values Fig. 2 Respiratory exchange ratio (RER) values and standard deviation at peak exercise in the three study groups P = 0.099 _ 2 /kg (ml/kg/min) VO _ 2 /kg (ml/kg/min) VCO _ VCO _ 2 VE/ P = 0.000 Eur J Appl Physiol Eur J Appl Physiol _ 2 We evaluated if the algorithm used to measure VCO could be affected by the respiratory pattern and there_ 2 fore our results could be influenced by the VCO _ 2 in the Sensor Medics Vmax calculation technique. VCO 29C is measured according to the following formula: _ 2 = STP 9 (FeCO2 - FiCO2) 9 RR/(1 - FeCO2 + VCO FiCO2/RER). The RR appears in the numerator of the formula so that subjects with higher RR (Group 2) should _ 2 . However, our have, if anything, a higher measured VCO results were the opposite, so that the algorithm used was _ 2 differences. not the cause of the observed VCO The decision to subdivide our study population into three different groups, using PETCO2 values obtained at RC, was taken to evaluate the role of ventilatory patterns on exercise performance. Indeed, RC is the exercise stage featuring the highest PETCO2 and is also the exercise stage less influenced by the volitional component of exercise ventilatory regulation and exercise performance (Wasserman et al. 2005). It should be stressed that PETCO2 is a marker, which combines exercise performance and efficiency of ventilation and by no means can be considered an independent physiological variable (see ‘‘Introduction’’). PETCO2 is used as a non-invasive measure of PaCO2 (Johnson et al. 1992; Wasserman 1978) in subjects with no evidence of cardiac and lung diseases and is most useful and indicative of PaCO2 when phase 3 of expiration is virtually flat, a situation that may not pertain to heavy exercise (Jones et al. 1979; Wasserman 1978). A high PaCO2 is considered a sign of inadequate hyperventilation (Dempsey and Wagner 1999; Martin et al. 1979) and of exercise limitation due to the respiratory system if a subject is near his maximal voluntary ventilation. However, and apparently in contradiction with the previous statement, subjects belonging to the lowest tertile of PETCO2 and therefore to the lowest value of PaCO2, achieved the lowest _ 2 during exercise. peak workload and VO Subjects with the lowest PETCO2, and probably lowest PaCO2, are likely to have the greatest exercise-induced acidosis, which explains the reduced exercise capacity. Why Group 2 and 3 have a different ventilatory pattern is much less clear but, in our opinion, very interesting. Group _ 2 2 and 3 reached the same exercise performance (same VO and workload) but in Group 3, PETCO2, by definition, and _ 2 , unexpectedly, were both higher at peak exercise. VCO Several explanations for these results are possible. The ventilatory pattern of subjects with higher PETCO2 at RC is peculiar and featured high Vt and low RR throughout _ was registered between Group exercise, albeit a similar VE 2 and 3. This ventilatory pattern, well described in endurance athletes, offers less expenditure of ventilation in dead space and, therefore, minor work of respiratory muscles (Clark et al. 1983; Johnson et al. 1992). This pattern could be related to a reduced chemoreceptor sensitivity associated with a lower dyspnoea feeling (Rodman et al. 2002; Takano et al. 1997). Harms et al. showed that minor tiredness in respiratory muscles, which can be experimentally obtained by mechanical unloading of these _ 2 muscles, allows for a reduction of respiratory muscles VO and blood flow and that this phenomenon is associated with more than 10% leg blood flow increase (Harms et al. 1995; Harms et al. 1997). Moreover, the same Authors suggested that the reduction of respiratory muscles workload and the increase in peripheral muscles flow, delays the feeling of dyspnoea, allowing a more advanced exercise load (Harms et al. 1998). According to this theory, Group 3 subjects should have registered a greater exercise performance than Group 1 and 2, but we observed that Group 2 and 3 have the same exercise capacity. We assume that Group 3 subjects were less fit subjects compared to those of Group 2. Indeed, subjects in the third tertile of PETCO2 had greater RER and _ 2 , suggesting an increased glycolytic metabolism peak VCO during exercise. Moreover, albeit not statistically different, anaerobic threshold showed a trend of lower work rates in Group 3 vs. Group 2. However, our hypothesis needs to be verified by a study on the effects of respiratory pattern as a guide to exercise training. Our hypothesis that subjects with high PETCO2 present a reduced ventilation response to exercise-induced CO2 accumulation is strengthened by the iso-watt analysis of ventilatory pattern during exercise. Indeed, starting from 100 W, subjects with higher PETCO2 at RC showed lower _ and of RR compared to Group 1 and a trend values of VE toward a higher Vt and lower RR compared to Group 2. _ of each of the Furthermore, if all data, all RR, Vt and VE iso-watt analysis are averaged, the ventilatory pattern difference between groups is clear, with lower RR and _ in higher Vt in Group 3, even if there is a similar VE Group 2 and 3. A few study limitations should be recognized. Firstly, our research suffers an absence of blood gas analysis and plasmatic lactate concentration values. Indeed, differences between blood and end-tidal CO2 data are likely not to be the same in comparing slow and fast breathing subjects. Blood gas data, which certainly would have been useful to support our findings, were not collected. However, Wasserman et al. (1978) reported a difference between PaCO2 and PETCO2 values of approximately +2.5 mmHg at rest to -4 mmHg during heavy work, which is below the difference in PETCO2 that we observed. Moreover, Jones et al. (1979) formulated an equation to predict PaCO2 directly from PETCO2 values. All these works support a good reliability of PETCO2 as an indirect measure of PaCO2 in healthy subjects (Benallal and Busso 2000). However, our study was aimed at investigating the relationship between physical performance and PETCO2 123 Eur J Appl Physiol considered as a marker, which combines efficiency of ventilation and exercise performance and not simply as an indicator of PaCO2. Secondly, we used a cycloergometer. Therefore, we do not know if the observed respiratory pattern is also present in exercise performed with other ergometers e.g. a treadmill. Thirdly, the cardiopulmonary tests were performed in our laboratory randomly during the year, without taking the subjects’ training period into consideration. This could be an important point of remark, because training modifies the respiratory pattern through an alteration of chemo and muscular receptors responsiveness. Fourthly, the population we analysed was a mixed population of physically well-trained subjects who practised varied sports and were therefore not athletes in a specific area. So our data needs to be confirmed for each specific sport. _ behaviour occurs through Finally, because specific VE the entire exercise and is present even at rest (see differences in resting PETCO2), it is possible, but totally unproven, that in the well-trained subjects, the ventilatory pattern pertains to regular life activity and not only to maximal exercise performance. In conclusion, in a healthy physically well-trained population, PETCO2 values during exercise could be useful in identifying particular respiratory patterns and their underlying physiological mechanisms. This parameter, which is easily and non-invasively detectable with a cardiopulmonary exercise test, could represent a tool in future studies on the relationship between ventilation and exercise performance. Indeed, it might be that subjects with the highest PETCO2 could, with training, improve their exercise performance more than the participants in Group 2. Consequently, our study raises more questions than it provided answers. Further studies are certainly required to evaluate if and how training affects the respiratory pattern during exercise and whether PETCO2 analysis during exercise can drive training methodologies. Acknowledgment We are indebted to Prof. Brian Whipp for the constructive critiques during preparation of the manuscript. 123 References Beaver WR, Wasserman K, Whipp BJ (1986) A new method for detecting the anaerobic threshold by gas exchange. J Appl Physiol 60:2020–2027 Benallal H, Busso T (2000) Analysis of end-tidal and arterial PCO2 gradients using a breathing model. Eur J Appl Physiol 83(4– 5):402–408 Clark JM, Hagerman FC, Gelfand R (1983) Breathing patterns during submaximal and maximal exercise in elite oarsmen. J Appl Physiol 55:440–446 Dempsey JA, Wagner PD (1999) Exercise-induced arterial hypoxemia. J Appl Physiol 87:1997–2006 Durand F, Mucci P, Prefaut C (2000) Evidence for an inadequate hyperventilation inducing arterial hypoxemia at submaximal exercise in all highly trained endurance athletes. Med Sci Sports Exer 32(5):926–932 Harms CA, Stager JM (1995) Low chemoresponsiveness and inadequate hyperventilation contribute to exercise-induced hypoxemia. J Appl Physiol 79:575–580 Harms CA, Babcock MA, McClaran SR et al (1997) Respiratory muscle work compromises leg blood flow during maximal exercise. J Appl Physiol 82(5):1573–1583 Harms CA, Wetter TJ, McClaran SR et al (1998) Effects of respiratory muscle work on cardiac output and its distribution during maximal exercise. J Appl Physiol 85(2):609–618 Harms CA, Wetterb TJ, St. Croix CM et al (2000) Effects of respiratory muscle work on exercise performance. J Appl Physiol 89:131–138 Johnson BD, Saupe KW, Dempsey JA (1992) Mechanical constraints on exercise hyperpnea in endurance athletes. J Appl Physiol 73:874–886 Jones NL, Robertson DG, Kane JW (1979) Difference between endtidal and arterial PCO2 in exercise. J Appl Physiol 47(5):954– 960 Martin BJ, Sparks KE, Zwillich CW et al (1979) Low exercise ventilation in endurance athletes. Med Sci Sports 11(2):181–185 Rodman JR, Haverkamp HC, Gordon SM et al (2002) Cardiovascular and respiratory system responses and limitations to exercise. In: Weisman IM, Zeballos RJ (eds) Clinical exercise testing. Prog Respir Res Karger, vol 32, Basel Takano N, Inaishi S, Zhang Y (1997) Individual differences in breathlessness during exercise, as related to ventilatory chemosensitivities in humans. J Physiol 499.3:843–848 Wasserman K (1978) Breathing during exercise. Physiology in Medicine series. N Engl J Med 298:780–785 Wasserman K, Hansen JE, Sue DY et al. (2005) Normal values. Arterial and end-tidal carbon dioxide tensions. In: Wasserman K, Hansen JE, Sue DY et al (eds) Principles of exercise testing and interpretation, 4th edn. Lippincott Williams & Wilkins, Philadelphia
© Copyright 2026 Paperzz